The TOR pathway comes of age

Biochim Biophys Acta. 2009 Oct;1790(10):1067-74. doi: 10.1016/j.bbagen.2009.06.007. Epub 2009 Jun 16.

Abstract

Studies in a variety of model organisms indicate that nutrient signaling is tightly coupled to longevity. In nutrient replete conditions, organisms develop, grow, and age quickly. When nutrients become sparse as with dietary restriction, growth and development decline, stress response pathways become induced and organisms live longer. Considerable effort has been devoted to understanding the molecular events mediating lifespan extension by dietary restriction. One central focus has been on nutrient-responsive signal transduction pathways including insulin/IGF-1, AMP kinase, protein kinase A and the TOR pathway. Here we describe the increasingly prominent links between TOR signaling and aging in invertebrates. Longevity studies in mammals are not published to date. Instead, we highlight studies in mouse models, which indicate that dampening the TOR pathway leads to widespread protection from an array of age-related diseases.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Aging / genetics
  • Aging / metabolism*
  • Animals
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism
  • Humans
  • Mice
  • Models, Biological
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Kinases / genetics
  • Protein Kinases / metabolism*
  • Signal Transduction*
  • TOR Serine-Threonine Kinases

Substances

  • Drosophila Proteins
  • Protein Kinases
  • target of rapamycin protein, Drosophila
  • MTOR protein, human
  • mTOR protein, mouse
  • TOR Serine-Threonine Kinases